李盈,高健美,白鑫宇,杨晓峰,李建春
LI Ying,GAO Jian-mei,BAI Xin-yu,YANG Xiao-feng,LI Jian-chun

• 1:沈阳药科大学生命科学与生物制药学院
• 2:山东万杰医学院医学系

摘要(Abstract)：

目的研究金丝桃苷对人正常肝细胞HL7702氧化损伤的保护作用及作用机制。方法采用乙醇诱导建立氧化损伤模型,MTT法检测细胞存活率,利用相关试剂盒检测ROS、SOD、MDA、GSH水平,rhodamine 123染色考察线粒体膜电位的变化,PI染色检测细胞凋亡程度,以及Western blot评价线粒体途径相关蛋白表达。结果确定100mmol·L-1乙醇为适宜浓度建立氧化损伤模型,形态学观察发现细胞变圆并悬浮于培养液中,PI染色显示细胞发生凋亡。100μmol·L-1金丝桃苷能够降低乙醇诱导的HL7702细胞中MDA的产生,提高SOD活力。同时,使促凋亡蛋白Bax、细胞色素c(cytochrome c)、caspase 3蛋白表达降低,增加抗凋亡蛋白Bcl-2蛋白表达。结论金丝桃苷可以保护乙醇诱导的肝细胞氧化损伤,其作用机制可能与抑制线粒体途径凋亡相关。
Objective To investigate the protective effects and the mechanisms of hyperoside on HL7702 cells injury induced by ethanol.Methods The oxidative cellular responses were induced by exposure to ethanol.MTT method,rhodamine 123 staining,PI staining and Western blot were applied.The reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD),glutathione(GSH)were measured.Results Compared with the controls,ethanol(100 mmol·L-1)treatment significantly increase ROS generation,MDA production,and induced apoptosis.While hyperoside(100μmol·L-1)co-incubation significantly increased the activity of SOD and GSH production.The release of cytochrome c from mitochondria was reduced by hyperoside,which increased the expression of antiapoptotic Bcl-2 and decreased the expression of Bax,cytochrome c,and caspase 3.Conclusions Hyperoside modulate the oxidative stress-induced apoptosis in HL7702 cells,probably due to its antioxidant activity and functioning via mitochondria-dependent pathways.

关键词(KeyWords)： 金丝桃苷;HL7702;氧化损伤;乙醇
hyperoside;HL7702;oxidative damage;ethanol

Abstract:

Keywords:

基金项目(Foundation):

作者(Author): 李盈,高健美,白鑫宇,杨晓峰,李建春
LI Ying,GAO Jian-mei,BAI Xin-yu,YANG Xiao-feng,LI Jian-chun

DOI: 10.14066/j.cnki.cn21-1349/r.2013.09.009

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